Previous studies in this laboratory have shown that mice treated with Concanavalin A prior to and at frequent intervals after challenge with an oncogenic viral agent (MSV), a chemical carcinogen (MCA) or an established tumor cell line (TEPC-15) showed a significant enhancement of tumor induction and/or development n all three systems. We propose to investigate the mechanism of this enhancement by comparing the humoral and cellular immune responses of treated versus control animals to the tumors. Subsequent studies will attempt to elucidate the cell-cell interactions involved in the observed enhancement. these studies will include in vitro separation of in vivo Con A activated spleen cells into subpopulations of T helper or T suppressor cells, and repopulation of irradiated or supplementation of normal mice with lymphocyte subpopulations of known effector function. In addition, the role of macrophages will be studied in similar experiments or by ablation of macrophage function in vivo by injection of silica. Depletion of T suppressor cels with I-J alloantisera will also be studied in an attempt to implicate Con A activated T suppressor cells in the observed enhancement phenomenon. Extension of these investigations to other lectins known to interact with lymphocyte subpopulations and to other oncogenic agents will also be done as time and funds permit.